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- W2892380681 abstract "Sodium butyrate (NaB), a histone deacetylase (HDAC) inhibitors, has been reported to attenuate hyperglycemia in rats. Our objective was to explore the effect and underlying mechanism of NaB on islet β-cell dysfunction and apoptosis in type 2 diabetic (T2DM) rats. T2DM models were induced by the combination of streptozotocin (STZ, 40 mg/kg) and high-fat-diet, while NaB (500 mg/kg/d) was intraperitoneally injected for 6 weeks in experimental groups. Our results suggested NaB mitigated hyperglycemia, lowered the levels of serum cholestenone (TC) and low-density lipoprotein (LDL-c), prevented body weight loss, and enhanced insulin resistance and glucose tolerance. NaB also improved diabetes-induced histological alteration of islet and functional damage; moreover, results of TUNEL and western blotting indicated NaB alleviated β-cell apoptosis. Further research showed NaB down-regulated the expression of endoplasmic reticulum stress (ERS) related proteins, including phosphorylated type I transmembrane ER-resident protein kinase (p-PERK), phosphorylated eukaryotic initiation factor 2α (p-eIF2α), activating transcription factor (ATF4) and CCAAT/enhancer-binding protein homologous protein (CHOP). Consequently, NaB mitigates type 2 diabetes by inhibiting PERK-CHOP pathway of ERS." @default.
- W2892380681 created "2018-09-27" @default.
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- W2892380681 date "2018-12-01" @default.
- W2892380681 modified "2023-09-26" @default.
- W2892380681 title "Sodium butyrate mitigates type 2 diabetes by inhibiting PERK-CHOP pathway of endoplasmic reticulum stress" @default.
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- W2892380681 doi "https://doi.org/10.1016/j.etap.2018.09.002" @default.
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